Fig. 3.
Kcna2 antisense (AS) RNA up-regulation specifically and selectively targets Kcna2 expression in neuropathic pain. (A) Under normal conditions, due to highly low expression of Kcna2 AS RNA, Kcna2 messenger RNA (mRNA) that is transcribed from the genome is translated into protein, resulting in the expression of the Kcna2 channel at the cell membrane. (B) Under neuropathic pain conditions, peripheral nerve injury promotes the expression of Kcna2 AS RNA that is transcribed from the opposing strand of the Kcna2 gene. Increased expression of Kcna2 AS RNA specifically and selectively inhibits expression of Kcna2 mRNA via extensive overlap of their complementary regions, including the transcription and translation inhibition sites, leading to reduced expression levels of the membrane Kcna2 channel only, not other Kcna family members (e.g., Kcna1).

Kcna2 antisense (AS) RNA up-regulation specifically and selectively targets Kcna2 expression in neuropathic pain. (A) Under normal conditions, due to highly low expression of Kcna2 AS RNA, Kcna2 messenger RNA (mRNA) that is transcribed from the genome is translated into protein, resulting in the expression of the Kcna2 channel at the cell membrane. (B) Under neuropathic pain conditions, peripheral nerve injury promotes the expression of Kcna2 AS RNA that is transcribed from the opposing strand of the Kcna2 gene. Increased expression of Kcna2 AS RNA specifically and selectively inhibits expression of Kcna2 mRNA via extensive overlap of their complementary regions, including the transcription and translation inhibition sites, leading to reduced expression levels of the membrane Kcna2 channel only, not other Kcna family members (e.g., Kcna1).

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